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CLINICALFEATURE
physician’s recommendation, available facilities, dentist
expertise, and patient’s oral, medical, and general condition.
(Scully C 2002)
Contraindications
The following are contraindicated:
Aspirin should be avoided by those known to be allergic to
NSAIDs. Nonsteroid anti-inflammatory drugs (NSAID)
crossreact with aspirin in aspirin-sensitive patients and vice
versa (Settipane GA. 1998). Caution should be exercised in
those with asthma or NSAID-precipitated bronchospasm due to
the inhibition of COX in airways of the sensitive patients
.patients with peptic ulcers are also encouraged to avoid
aspirin. Children, including teenagers, are discouraged from
using aspirin in cold or flu symptoms as this has been linked
with Reye’s syndrome (MacDonald S 2002). Patients with other
bleeding tendencies are also recommended to avoid aspirin.
Aspirin-Induced Asthma, (AIA) has been reported. The
frequency among asthmatics is around 8%-20%. Aspirin blocks
the enzyme cyclooxygenase and this reduces the synthesis of
prostaglandins. A further potential result of this blockade
however is to shunt the cascade of reactions into a leukotriene
pathway and leukotrienes are known to induce
bronchoconstriction. Other theories are based on AIA patients
having abnormal platelets, having abnormal thromboxane/
prostaglandin ratios in the lung or even having had a chronic
viral infection.
NSAIDs (including COX II), is the acronym for Non-Steroidal
Anti-Inflammatory Drugs. They are peripherally-acting antipyretic
analgesic anti-inflammatory drug.
The latest addition are the COX II inhibitors, introduced in
1998. It acts via the inhibition of the enzyme cyclooxygenase
which in turn reduces the level of prostaglandins in the body.
Therefore, it is a peripherally-acting antipyretic analgesic anti
inflammatory drug. Likewise, it has weak anti-thrombotic effect,
being a weak inhibitor of platelet aggregation. It is also safer on
the stomach than aspirin . Cyclooxygenase, is an enzyme that
occurs in at least two isoforms:
1) COX1 (constitutive), which mediates formation of
prostaglandins responsible for GI mucosal protection,
hemostasis and renal blood flow.
2) COX2 (inducible), which catalyzes production of
prostaglandins that act as inflammatory mediators. The
enzyme can play a homeostatic role in some situations
(ulcer healing, maintenance of renal blood flow during
stress, prostacyclin production).In general NSAID’s that
inhibit COX2>COX1 are considered the drugs of choice in
this class.
The following are some common NSAIDs
1. Diclofenac
There is no clear evidence that
taking paracetamol causes
asthma, but more studies are
suggesting that may be some
association
2. Diflunisal
3. Etodolac
4. Fenoprofen
5. Floctafenine
6. Flurbiprofen
7. Ibuprofen
8. Indomethacin
9. Ketoprofen
10. Meclofenamate
11. Mefenamic Acid
12. Meloxicam
13. Nabumetone
14. Naproxen
15. Oxaprozin
16. Phenylbutazone
17. Piroxicam
18. Sulindac
19. Tenoxicam
20. Tiaprofenic Acid
21. Tolmetin
The COX II Inhibitors include the following:
1. Celecoxib Celebrex®
2. Rofecoxib Vioxx®*
3. Valdecoxib Bextra*
4. Etoricoxib Arcoxia
* withdrawn from market
The drugs are recommended for use on patients with allergic
reaction to aspirin or has had urticaria, rhinitis or asthma
associated with NSAIDs .NSAID’s should be avoided in the
presence of renal or hepatic dysfunction, coagulopathies, GI
disorders, shock, hypotension/hypovolemia, hypoalbuminemia
or pregnancy.
In the Vioxx Gastrointestinal Outcomes Research (VIGOR)
trial, there was a higher incidence of cardiovascular thrombotic
events in the rofecoxib vs the naproxen-treated group: 1.67 vs
0.70 per 100 patient years. (Konstam 2002)
In a comprehensive analysis of 114 randomized trials with
116,094 participants, rofecoxib was associated with increased
Dental Asia • May / June 2008
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